Craniofacial Morphology in Myostatin-deficient Mice

2007 ◽  
Vol 86 (11) ◽  
pp. 1068-1072 ◽  
Author(s):  
L. Vecchione ◽  
C. Byron ◽  
G.M. Cooper ◽  
T. Barbano ◽  
M.W. Hamrick ◽  
...  
Keyword(s):  
Masseter Muscle ◽  
Shape Index ◽  
Craniofacial Morphology ◽  
Cranial Vault ◽  
Muscle Size ◽  
Masticatory Muscle ◽  
Wild Type ◽  
Muscle Weight ◽  
Mandibular Body ◽  
Deficient Mice

GDF-8 (myostatin) is a negative growth regulator of skeletal muscle, and myostatin-deficient mice are hypermuscular. Muscle size and force production are thought to influence growth of the craniofacial skeleton. To test this relationship, we compared masticatory muscle size and craniofacial dimensions in myostatin-deficient and wild-type CD-1 control mice. Myostatin-deficient mice had significantly (p < 0.01) greater body (by 18%) and masseter muscle weight (by 83%), compared with wild-type controls. Significant differences (p < 0.05) were noted for cranial vault length, maxillary length, mandibular body length, and mandibular shape index. Significant correlations were noted between masseter muscle weight and mandibular body length (r = 0.68; p < 0.01), cranial vault length (r = −0.57; p < 0.05), and the mandibular shape index (r = −0.56; p < 0.05). Masticatory hypermuscularity resulted in significantly altered craniofacial morphology, probably through altered biomechanical stress. These findings emphasize the important role that masticatory muscle function plays in the ontogeny of the cranial vault, the maxilla, and, most notably, the mandible.

scholarly journals Endocranial and masticatory muscle volumes in myostatin-deficient mice

2014 ◽  
Vol 1 (4) ◽  
pp. 140187 ◽  
Author(s):  
Nathan Jeffery ◽  
Christopher Mendias
Keyword(s):  
Brain Size ◽  
Masticatory Muscles ◽  
Muscle Size ◽  
Masticatory Muscle ◽  
Cavalieri Principle ◽  
Trade Offs ◽  
Contrast Enhanced ◽  
Endocranial Volume ◽  
Deficient Mice ◽  
Total Muscle

Structural and functional trade-offs are integral to the evolution of the mammalian skull and its development. This paper examines the potential for enlargement of the masticatory musculature to limit the size of the endocranial cavity by studying a myostatin-deficient mouse model of hypermuscularity (MSTN−/−). The study tests the null prediction that the larger MSTN−/− mice have larger brains compared with wild-type (WT) mice in order to service the larger muscles. Eleven post-mortem MSTN−/− mice and 12 WT mice were imaged at high resolution using contrast enhanced micro-CT. Masticatory muscle volumes (temporalis, masseter, internal and external pterygoids) and endocranial volumes were measured on the basis of two-dimensional manual tracings and the Cavalieri principle. Volumes were compared using Kruskal–Wallis and Student's t -tests. Results showed that the masticatory muscles of the MSTN−/− mice were significantly larger than in the WT mice. Increases were in the region of 17–36% depending on the muscle. Muscles increased in proportion to each other, maintaining percentages in the region of 5, 10, 21 and 62% of total muscle volume for the external ptyergoid, internal pterygoid, temporalis and masseter, respectively. Kruskal–Wallis and t -tests demonstrated that the endocranial volume was significantly larger in the WT mice, approximately 16% larger on average than that seen in the MSTN−/− mice. This comparative reduction of MSTN−/− endocranial size could not be explained in terms of observer bias, ageing, sexual dimorphism or body size scaling. That the results showed a reduction of brain size associated with an increase of muscle size falsifies the null prediction and lends tentative support to the view that the musculature influences brain growth. It remains to be determined whether the observed effect is primarily physical, nutritional, metabolic or molecular in nature.

Different effects of chronic helicobactor pylori infection on parietal and ECL cells between wild type and gastrin-deficient mice

2001 ◽  
Vol 120 (5) ◽  
pp. A728-A728
Author(s):  
D CHEN ◽  
L FRIISHANSEN ◽  
X WANG ◽  
C ZHAO ◽  
H WALDUM ◽  
...  
Keyword(s):  
Wild Type ◽  
Ecl Cells ◽  
Helicobactor Pylori ◽  
Deficient Mice

CCR5 deficiency decreases susceptibility to experimental cerebral malaria

Blood ◽  
2003 ◽  
Vol 101 (11) ◽  
pp. 4253-4259 ◽  
Author(s):  
Elodie Belnoue ◽  
Michèle Kayibanda ◽  
Jean-Christophe Deschemin ◽  
Mireille Viguier ◽  
Matthias Mack ◽  
...  
Keyword(s):  
T Cells ◽  
Cerebral Malaria ◽  
Cd8 T Cells ◽  
Cytokine Production ◽  
Wild Type ◽  
Experimental Cerebral Malaria ◽  
Pathologic Features ◽  
Th1 Cytokine ◽  
The Brain ◽  
Deficient Mice

Abstract Infection of susceptible mouse strains with Plasmodium berghei ANKA (PbA) is a valuable experimental model of cerebral malaria (CM). Two major pathologic features of CM are the intravascular sequestration of infected erythrocytes and leukocytes inside brain microvessels. We have recently shown that only the CD8+ T-cell subset of these brain-sequestered leukocytes is critical for progression to CM. Chemokine receptor–5 (CCR5) is an important regulator of leukocyte trafficking in the brain in response to fungal and viral infection. Therefore, we investigated whether CCR5 plays a role in the pathogenesis of experimental CM. Approximately 70% to 85% of wild-type and CCR5+/- mice infected with PbA developed CM, whereas only about 20% of PbA-infected CCR5-deficient mice exhibited the characteristic neurologic signs of CM. The brains of wild-type mice with CM showed significant increases in CCR5+ leukocytes, particularly CCR5+ CD8+ T cells, as well as increases in T-helper 1 (Th1) cytokine production. The few PbA-infected CCR5-deficient mice that developed CM exhibited a similar increase in CD8+ T cells. Significant leukocyte accumulation in the brain and Th1 cytokine production did not occur in PbA-infected CCR5-deficient mice that did not develop CM. Moreover, experiments using bone marrow (BM)–chimeric mice showed that a reduced but significant proportion of deficient mice grafted with CCR5+ BM develop CM, indicating that CCR5 expression on a radiation-resistant brain cell population is necessary for CM to occur. Taken together, these results suggest that CCR5 is an important factor in the development of experimental CM.

scholarly journals Toll-like Receptor 4 Signaling in Ventilator-induced Diaphragm Atrophy

2012 ◽  
Vol 117 (2) ◽  
pp. 329-338 ◽  
Author(s):  
Willem-Jan M. Schellekens ◽  
Hieronymus W. H. van Hees ◽  
Michiel Vaneker ◽  
Marianne Linkels ◽  
P. N. Richard Dekhuijzen ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Caspase 3 ◽  
Toll Like Receptor ◽  
Wild Type ◽  
Toll Like Receptor 4 ◽  
Ubiquitin Proteasome Pathway ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway ◽  
Diaphragm Atrophy ◽  
Deficient Mice

Background Mechanical ventilation induces diaphragm muscle atrophy, which plays a key role in difficult weaning from mechanical ventilation. The signaling pathways involved in ventilator-induced diaphragm atrophy are poorly understood. The current study investigated the role of Toll-like receptor 4 signaling in the development of ventilator-induced diaphragm atrophy. Methods Unventilated animals were selected for control: wild-type (n = 6) and Toll-like receptor 4 deficient mice (n = 6). Mechanical ventilation (8 h): wild-type (n = 8) and Toll-like receptor 4 deficient (n = 7) mice.Myosin heavy chain content, proinflammatory cytokines, proteolytic activity of the ubiquitin-proteasome pathway, caspase-3 activity, and autophagy were measured in the diaphragm. Results Mechanical ventilation reduced myosin content by approximately 50% in diaphragms of wild-type mice (P less than 0.05). In contrast, ventilation of Toll-like receptor 4 deficient mice did not significantly affect diaphragm myosin content. Likewise, mechanical ventilation significantly increased interleukin-6 and keratinocyte-derived chemokine in the diaphragm of wild-type mice, but not in ventilated Toll-like receptor 4 deficient mice. Mechanical ventilation increased diaphragmatic muscle atrophy factor box transcription in both wild-type and Toll-like receptor 4 deficient mice. Other components of the ubiquitin-proteasome pathway and caspase-3 activity were not affected by ventilation of either wild-type mice or Toll-like receptor 4 deficient mice. Mechanical ventilation induced autophagy in diaphragms of ventilated wild-type mice, but not Toll-like receptor 4 deficient mice. Conclusion Toll-like receptor 4 signaling plays an important role in the development of ventilator-induced diaphragm atrophy, most likely through increased expression of cytokines and activation of lysosomal autophagy.

scholarly journals Anatomical Characteristics of the Masseter Muscle in Mandibular Prognathism

2021 ◽  
Vol 11 (10) ◽  
pp. 4444
Author(s):  
Ji Ho Yang ◽  
Dong Sun Shin ◽  
Jeong-Hun Yoo ◽  
Hun Jun Lim ◽  
Jun Lee ◽  
...  
Keyword(s):  
Masseter Muscle ◽  
Normal Group ◽  
Length Ratio ◽  
Mandibular Prognathism ◽  
Anatomical Characteristics ◽  
Mandibular Plane ◽  
Mandibular Body ◽  
The Difference

Mandibular prognathism causes functional and esthetic problems. Therefore, many studies have been conducted to understand its etiology. Following our previous study, which revealed that the major characteristic of the mandible with prognathism is the volume/length ratio of the mandibular body and condyle, we analyzed the volume and orientation of the masseter muscle, which inserts into the mandibular body, expecting that the difference in the size of the masseter muscle causes the difference in the mandibular size. This study compared the masseter muscle of the participants in the prognathic group to those in the normal group on the volume/length ratio and orientation. The masseter muscle ratios (volume/length); the angle between the superficial and deep head of the masseter muscle; and the three planes (the palatal, occlusal, and mandibular) were analyzed. A total of 30 participants constituted the normal group (male: 15, female: 15) and 30 patients, the prognathic group (male: 15, female: 15). The results showed that the volume/length ratio of the masseter of the normal group was greater than that of the prognathic group (p < 0.05). In addition, the orientation of both the superficial and deep head of the masseter of the participants in the normal group was more vertical with respect to the mandibular plane than that of the prognathic group (p < 0.05). We concluded that the mechanical disadvantage of the masseter muscle of the prognathic group is attributed to mandibular prognathism.

A High Masticatory Muscle Tone Predicts the Risk of Malnutrition and Frailty in Inpatient Older Adults: A Cross-Sectional Study

Gerontology ◽  
2021 ◽  
pp. 1-7
Author(s):  
Yin-Hwa Shih ◽  
Zhen-Rong Hong ◽  
Shih-Min Hsia ◽  
Shang-Yu Yang ◽  
Tzong-Ming Shieh
Keyword(s):  
Older Adults ◽  
At Risk ◽  
Nutritional Status ◽  
Masseter Muscle ◽  
Muscle Tone ◽  
Handgrip Strength ◽  
Muscle Performance ◽  
Masticatory Muscle ◽  
Masticatory Performance ◽  
Poor Nutritional Status

<b><i>Introduction:</i></b> The prevalence of malnutrition among inpatient older adults is as high as 20∼50%. Masticatory performance is known to affect the nutritional status of individuals. However, an objective measurement to reflect the real status of masticatory muscle performance is lacking at the bedside. <b><i>Methods:</i></b> This pilot study analyzed the masticatory performance using surface electromyography (sEMG) of masticatory muscles that measures both muscle strength and muscle tone at the bedside. The nutritional status was measured using the Mini Nutritional Assessment tool. The handgrip strength was measured using a hand dynamometer. The statistical data were analyzed using SPSS 25 software. <b><i>Results:</i></b> The data revealed that female inpatient older adults more frequently had substandard handgrip strength (<i>p</i> = 0.028), an at-risk and poor nutritional status (<i>p</i> = 0.005), and a higher masseter muscle tone (<i>p</i> = 0.024). Inpatient older adults with an at-risk and poor nutritional status had an older age (<i>p</i> = 0.016), lower handgrip strength (<i>p</i> = 0.001), and higher average masseter muscle tone (<i>p</i> = 0.01). A high masseter muscle tone predicted the risk of having an at-risk and poor nutritional status. The at-risk or poor nutritional status predicted having a substandard handgrip strength by 5-fold. <b><i>Conclusions:</i></b> A high masticatory muscle tone predicts malnutrition and frailty. Medical professionals should combat masticatory dysfunction-induced malnutrition by detecting masticatory muscle performance using sEMG and referring patients to dental professionals. Additionally, encouraging inpatient older adults to perform oral motor exercise is recommended.

Vasomotor responses in MnSOD-deficient mice

2004 ◽  
Vol 287 (3) ◽  
pp. H1141-H1148 ◽  
Author(s):  
Jon J. Andresen ◽  
Frank M. Faraci ◽  
Donald D. Heistad
Keyword(s):  
Oxidative Stress ◽  
Acute Hypoxia ◽  
Vasomotor Response ◽  
Wild Type ◽  
Similar Extent ◽  
Sod Activity ◽  
Vasomotor Function ◽  
Mitochondrial Superoxide ◽  
Prostaglandin F ◽  
Deficient Mice

MnSOD is the only mammalian isoform of SOD that is necessary for life. MnSOD−/− mice die soon after birth, and MnSOD+/− mice are more susceptible to oxidative stress than wild-type (WT) mice. In this study, we examined vasomotor function responses in aortas of MnSOD+/− mice under normal conditions and during oxidative stress. Under normal conditions, contractions to serotonin (5-HT) and prostaglandin F2α (PGF2α), relaxation to ACh, and superoxide levels were similar in aortas of WT and MnSOD+/− mice. The mitochondrial inhibitor antimycin A reduced contraction to PGF2α and impaired relaxation to ACh to a similar extent in aortas of WT and MnSOD+/− mice. The Cu/ZnSOD and extracellular SOD inhibitor diethyldithiocarbamate (DDC) paradoxically enhanced contraction to 5-HT and superoxide more in aortas of WT mice than in MnSOD+/− mice. DDC impaired relaxation to ACh and reduced total SOD activity similarly in aortas of both genotypes. Tiron, a scavenger of superoxide, normalized contraction to 5-HT, relaxation to ACh, and superoxide levels in DDC-treated aortas of WT and MnSOD+/− mice. Hypoxia, which reportedly increases superoxide, reduced contractions to 5-HT and PGF2α similarly in aortas of WT and MnSOD+/− mice. The vasomotor response to acute hypoxia was similar in both genotypes. In summary, under normal conditions and during acute oxidative stress, vasomotor function is similar in WT and MnSOD+/− mice. We speculate that decreased mitochondrial superoxide production may preserve nitric oxide bioavailability during oxidative stress.

scholarly journals A role for CD9 molecules in T cell activation.

1996 ◽  
Vol 184 (2) ◽  
pp. 753-758 ◽  
Author(s):  
X G Tai ◽  
Y Yashiro ◽  
R Abe ◽  
K Toyooka ◽  
C R Wood ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Immune Responses ◽  
T Cell Activation ◽  
Cell Activation ◽  
Expression Cloning ◽  
Wild Type ◽  
Almost All ◽  
Antigen Presenting ◽  
Deficient Mice

Costimulation mediated by the CD28 molecule plays an important role in optimal activation of T cells. However, CD28-deficient mice can mount effective T cell-dependent immune responses, suggesting the existence of other costimulatory systems. In a search for other costimulatory molecules on T cells, we have developed a monoclonal antibody (mAb) that can costimulate T cells in the absence of antigen-presenting cells (APC). The molecule recognized by this mAb, 9D3, was found to be expressed on almost all mature T cells and to be a protein of approximately 24 kD molecular mass. By expression cloning, this molecule was identified as CD9, 9D3 (anti-CD9) synergized with suboptimal doses of anti-CD3 mAb in inducing proliferation by virgin T cells. Costimulation was induced by independent ligation of CD3 and CD9, suggesting that colocalization of these two molecules is not required for T cell activation. The costimulation by anti-CD9 was as potent as that by anti-CD28. Moreover, anti-CD9 costimulated in a CD28-independent way because anti-CD9 equally costimulated T cells from the CD28-deficient as well as wild-type mice. Thus, these results indicate that CD9 serves as a molecule on T cells that can deliver a potent CD28-independent costimulatory signal.

scholarly journals Altered V-ATPase expression in renal intercalated cells isolated from B1 subunit-deficient mice by fluorescence-activated cell sorting

2013 ◽  
Vol 304 (5) ◽  
pp. F522-F532 ◽  
Author(s):  
Luca Vedovelli ◽  
John T. Rothermel ◽  
Karin E. Finberg ◽  
Carsten A. Wagner ◽  
Anie Azroyan ◽  
...  
Keyword(s):  
Cell Sorting ◽  
Collecting Duct ◽  
Egfp Expression ◽  
Intercalated Cells ◽  
Wild Type ◽  
Western Blots ◽  
Atpase Subunit ◽  
Protein Levels ◽  
Baseline Conditions ◽  
Deficient Mice

Unlike human patients with mutations in the 56-kDa B1 subunit isoform of the vacuolar proton-pumping ATPase (V-ATPase), B1-deficient mice (Atp6v1b1−/−) do not develop metabolic acidosis under baseline conditions. This is due to the insertion of V-ATPases containing the alternative B2 subunit isoform into the apical membrane of renal medullary collecting duct intercalated cells (ICs). We previously reported that quantitative Western blots (WBs) from whole kidneys showed similar B2 protein levels in Atp6v1b1−/− and wild-type mice (Păunescu TG, Russo LM, Da Silva N, Kovacikova J, Mohebbi N, Van Hoek AN, McKee M, Wagner CA, Breton S, Brown D. Am J Physiol Renal Physiol 293: F1915–F1926, 2007). However, WBs from renal medulla (including outer and inner medulla) membrane and cytosol fractions reveal a decrease in the levels of the ubiquitous V-ATPase E1 subunit. To compare V-ATPase expression specifically in ICs from wild-type and Atp6v1b1−/− mice, we crossed mice in which EGFP expression is driven by the B1 subunit promoter (EGFP-B1+/+ mice) with Atp6v1b1−/− mice to generate novel EGFP-B1−/− mice. We isolated pure IC populations by fluorescence-assisted cell sorting from EGFP-B1+/+ and EGFP-B1−/− mice to compare their V-ATPase subunit protein levels. We report that V-ATPase A, E1, and H subunits are all significantly downregulated in EGFP-B1−/− mice, while the B2 protein level is considerably increased in these animals. We conclude that under baseline conditions B2 upregulation compensates for the lack of B1 and is sufficient to maintain basal acid-base homeostasis, even when other V-ATPase subunits are downregulated.

scholarly journals The Alopecia Areata Phenotype Is Induced by the Water Avoidance Stress Test In cchcr1-Deficient Mice

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 840
Author(s):  
Qiaofeng Zhao ◽  
Satoshi Koyama ◽  
Nagisa Yoshihara ◽  
Atsushi Takagi ◽  
Etsuko Komiyama ◽  
...  
Keyword(s):  
Alopecia Areata ◽  
Gene Knockout ◽  
Stress Test ◽  
Coiled Coil ◽  
Risk Haplotype ◽  
Gene Expression Microarray ◽  
Wild Type ◽  
Gene Knockout Mice ◽  
Deficient Mice ◽  
Gene Expression Microarray Analysis

We recently discovered a nonsynonymous variant in the coiled-coil alpha-helical rod protein 1 (CCHCR1) gene within the alopecia areata (AA) risk haplotype. We also reported that the engineered mice with this risk allele exhibited. To investigate more about the involvement of the CCHCR1 gene in AA pathogenesis, we developed an AA model using C57BL/6N cchcr1 gene knockout mice. In this study, mice (6–8 weeks) were divided into two groups: cchcr1−/− mice and wild-type (WT) littermates. Both groups were subjected to a water avoidance stress (WAS) test. Eight weeks after the WAS test, 25% of cchcr1−/− mice exhibited non-inflammatory foci of alopecia on the dorsal skin. On the other hand, none of wild-type littermates cause hair loss. The foci resembled human AA in terms of gross morphology, trichoscopic findings and histological findings. Additionally, gene expression microarray analysis of cchcr1−/− mice revealed abnormalities of hair related genes compared to the control. Our results strongly suggest that CCHCR1 is associated with AA pathogenesis and that cchcr1−/− mice are a good model for investigating AA.

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